The pathophysiology of cartilage diseases

Treatment of traumatic or degenerative defects of articular cartilage is a well-known problem for surgeons. Temporary or permanent disablement and high cost are due to diseases of the cartilage and bone. The articular cartilage is considered a tissue without the capacity to repair so that the "mechanical wear" of joint tissues is often designated as a normal tribute to increasing age.
Different diseases like osteoarthrosis, metabolic or neuropathic arthropathia, traumatic damage of cartilage have to be distinguished. All of them have an individual cause and on individual progress. However, it is necessary to understand the physiology and pathophysiology of cartilage diseases to create new forms of treatment. This article covers principles of cartilage breakdown.
The mechanical wear is often used to describe the aetiology of osteoarthrosis. Morphological changes of the synovial fluid can be observed in the end-stage of the disease. A hypertrophic phase in the beginning of osteoarthrosis does not lead to an accumulation of extracellular matrix because catabolic processes occur. The surface of articular cartilage becomes more vulnerable and a disruption of the superficial zone becomes possible. The destruction of cartilage is followed by changes of the subchondral bone and a disruption of the articular surface.
The depth of the cartilage defect is an important factor as well as the location in the joint to undernsand the pathophysiology of articular cartilage damage. An isolated fibrillation of the superficial zone may be without any consequences whereas deeper defects without a penetration of the subchondral bone are a well-known problem. A spontaneous regeneration does not occur since immigration of mesenchymal stem cells from the blood vessels is not possible.
Osteochondrosis dissecans is not a disease of the articular cartilage in the first place but a necrosis of the subchondral bone. Secondary articular cartilage can be involved and form free bodies of cartilage or cartilage and bone. The subchondral sclerosis hinders a spontaneous regeneration from the subchondral bone-marrow.
The knowledge of the poor spontaneous regeneration of articular cartilage has lead to the development of new therapeutic approaches and techniques. A critical discussion about the results of new procedures might be easier with a good knowledge of the pathophysiology of cartilage diseases.